Contact details +64 (06) 356 9099 ext. 84715
EDUCATION
Rutgers University - NJ, USA
Ph.D., Graduate program in Cell and Developmental Biology
Korea Advanced Institute of Science & Technology - Seoul, Korea
Master of Science in Biological Science and Engineering
RESEARCH EXPERIENCE
? Senior Lecturer, Massey University at Palmerston North, New Zealand 2009 - present
? Research Associate, Rockefeller University, NY, USA 2003 - 2009
? Research Staff, Princeton University, NJ, USA 1999 - 2003
? PhD Student, Rutgers, The State University of NJ 1994-1999
? Assistant Manager, R&D Department, Daewoon Pharmaceutical Co. Ltd. 1991-1994
? MS Student, KAIST 1989-1991
TEACHING
122.703 Gene Expression (teaching area: Transcription factors and cancer)
122.233 Metabolic Biochemistry (course coordinator, teaching area: regulation of metabolism and signal transduction pathways)
203.303 Gene Regulation (teaching area: transcriptional regulation in eukaryotes including epigenetics)
203.300 DNA technology (teaching area: Recombination and Transposition)
GRANT AWARDS
? Genesis Oncology Trust Cancer grant 2013 - 2014
? Massey University Research Fund 2013
? PNMRF Cancer grant 2011 – 2012
? Massey University Research Fund 2010 – 2011
? PNMRF Summer Scholarship for post-graduates 2009 – 2013
PUBLICATIONS
1. Tian Yang, Christopher Burrows, and Jeong hyeon Park* (2013) Development of a tetracycline-inducible lentiviral vector with an instant regulatory system. Manuscript submitted and Under review
2. Jeong hyeon Park* et.al (2013) PPM1B is a negative regulator of replicative cellular senescence of human IMR-90 fibroblasts. Manuscript submitted and under review.
3. Kangmoon Lee, Zin Zee Lau, Courtney Meredith and Jeong hyeon Park* (2012) Decrease of p400 ATPase complex and loss of H2A.Z within the p21 promoter occur in senescent IMR-90 human fibroblasts. Mech. Ageing dev. 133, 686-694 * corresponding author
4. Jeong hyeon Park* and Natisha Magan (2011) Reverse Transcriptase-coupled Quantitative Real Time PCR Analysis of Cell-free Transcription on the Chromatin-assembled p21 Promoter. PLOS One, 6 (8): e23617 *corresponding author
5. Jeong hyeon Park* et.al (2011) The GAS41-PP2Cβ complex dephosphorylates p53 at serine 366 and regulates its stability. J. Biol. Chem. 286, 10911-10917 *corresponding author
6. Jeong hyeon Park, Xiao-Jian Sun, and Robert G. Roeder (2010) The SANT domain of p400 ATPase represses acetyltransferase activity and coactivator function of TIP60 in basal p21 gene expression. Mol. Cell. Biol. 30, 2750-2761
7. Jeong hyeon Park and Robert G. Roeder (2006) GAS41 is required for repression of the p53 tumor suppressor pathway during normal cellular proliferation. Mol. Cell. Biol. 26, 4006-4016
8. Mikhail A. Nikiforov*, Sanjay Chandriani*, Jeong hyeon Park*, Lulia Kotenko, Dina Matheos, Anna Johnsson, Steven B. McMahon and Michael D. Cole (2002) TRRAP-dependent and TRRAP-independent transcriptional activation by the Myc oncoprotein. Mol. Cell. Biol. 22, 5054-5063 *equal contributors
9. Jeong hyeon Park, Marcelo A. Wood and Michael D. Cole (2002) BAF53 forms three distinct nuclear complexes and functions as a Critical c-Myc interacting nuclear cofactor for oncogenic transformation. Mol. Cell. Biol. 22, 1307-1316
10. Jeong hyeon Park, Sudeesha Kunjibettu, Steven B. McMahon, and Michael D. Cole (2001) The ATM- related domain of TRRAP is required for histone acetyltransferases recruitment and Myc-dependent oncogenesis. Genes & Dev. 15, 1619-1624
I am a Senior Lecturer in Mammalian Biochemistry at Massey University, Palmerston North.
I studied chromatin remodeling/modifying complexes in conjunction with the c-Myc oncogenic transcription factor during my postdoctoral training with Professor Michael D. Cole. Then, I joined to the Professor Robert Roeder’s Lab at Rockefeller University to extend my studies in the transcriptional regulation of eukaryotic genome with regard to the p53 tumor suppressor pathway. Currently I have three major research topics that are relevant to basic cancer biolgoy and biochemistry.
In vitro epigenetic studies in cell free system
The compaction of eukaryotic DNA within chromatin structures allows intricate multilevel regulatory response to diverse environmental signals through various chromatin modifications. The epigenetic regulatory mechanisms of gene expression include post-translational modifications of histone tails and specific incorporation of histone variants such as H2A.Z into the genome. We are interested in recapitulating p21 gene regulation with purified recombinant proteins and artificially assembled chromatin templates in test tubes. Currently, we are investigating MSK1 serine/threonine kinase that is known to be a histone H3 serine 10/28 kinase and that has been implicated in cancer, inflammation and neurodegenerative diseases. To find the phosphorylation sites on MSK1 being essentially required for MSK1 targeting to the promoter, we have established the system to generate 36 different mutations on MSK1 phosphorylation sites. Ultimately we will attempt to identify gain-of-function mutations of MSK1 that will contribute to the p53-dependent transcriptional activation and to a pathogenic mechanism of neurodegenerative disorders.
p400 ATP-dependent chromatin remodeller in DNA damage response
The TIP60 complex contains two major enzyme subunits among 16 subunit members. TIP60 is a histone acetyltransferase that plays diverse roles in DNA damage responses, DNA double strand break repair, and transcriptional regulation. The other enzyme, p400, is an ATPase that serves as an ATP-dependent chromatin remodelling enzyme. Our recent studies demonstrate that a SWI3-ADA2-N-CoR-TFIIIB (SANT) domain of p400 binds directly to the TIP60 and blocks both its enzymatic activity and p53-dependent coactivator function. We are currently investigating how p400 plays a role in regulating ATM serine/threonine kinase and TIP60 during DNA damage response and repair processes.
PPM1B in regulating p53 tumor suppressor
We recently identified the novel interaction of a brain cancer gene, GAS41 in potentially regulating Protein Phosphatase 2Cβ (PPM1B). To extend our finding, we are investigating the hypothesis that PPM1B is a critical regulator of cellular senescence. By using the lentiviral shRNA-mediated knockdown, we will attempt to see if the alteration of PPM1B levels or its regulator can suppress a brain tumor cell growth.
Health and Well-being
Field of research codes
Biochemistry and Cell Biology (060100):
Biological Sciences (060000):
Cancer Cell Biology (111201):
Cancer Genetics (111203):
Cell Development, Proliferation and Death (060103):
Enzymes (060107):
Epigenetics (incl. Genome Methylation and Epigenomics) (060404):
Genetics (060400):
Medical And Health Sciences (110000):
Oncology and Carcinogenesis (111200):
Proteomics and Intermolecular Interactions (excl. Medical Proteomics) (060109):
Signal Transduction (060111):
Synthetic Biology (060113)
Present research/professional specialty
My expertise includes basic cancer biology, protein biochemistry and epigenetic gene regulation. I am interested in DNA damage response focusing on the p53 tumor suppressor protein whose mutations or mis-regulations are major triggers in almost every form of human cancers. My group currently investigates p53-dependent eukaryotic gene regulation, post-translational modifications, and DNA damage-mediated signal transduction pathways. By combining tissue culture system with powerful biochemistry tools, my research group is looking for molecular targets to sensitize cancer cells to current chemo- and radio-therapy.
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